Male rats, 60 days old, were treated with chlordane during or after induction of liver cirrhosis with carbon tetrachloride to determine the effect of treatment with chlordane on the response of the rats to the disease. When liver cirrhosis was induced simultaneously with chlordane treatment the disease symptoms were aggravated; the lipid content of the tissue was lowered significantly, growth rate was significantly lower than controls and there was no apparent replacement of damaged liver tissue by liver growth. The cytochrome P450 content of the liver was similar after both treatments. Continuation of the chlordane treatment after termination of the carbon tetrachloride treatment brought about a more rapid recovery from the induced cirrhotic condition. All these responses were to a dose range one tenth the recommended "no effect" level for healthy animals.
The use of AHF in the rat as a predictive lesion for carcinogenesis has been frequently suggested. Regulatory agencies require that the data used to determine carcinogenic potential and for estimating risk cannot be open to different interpretations. The degree of uncertainty in establishing relationships between the different foci phenotypes, their fate, and the difference in results with different protocols precludes the use of these data is establishing carcinogenic hazard or in quantitative risk estimation.
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